Amrubicin ((+)-(7S,9S)-9-acetyl-9-amino-7-[(2-deoxy-β-D-erythro-pentopyranosyl)oxy]-7,8,9,10-tetrahydro-6,11-dihydroxy-5,12-naphthacenedione) is an anthracycline compound represented by the following chemical structural formula (JP 3-5397B, U.S. Pat. No. 4,673,668):

Amrubicin is easily reduced in vivo to form a metabolite (amrubicinol) which is a 13-hydroxylated product. This amrubicinol has a considerably stronger inhibitory activity against growth of tumor cells than that of amrubicin. Doxorubicin and daunomycin, the other anthracycline compounds, also form reduced metabolites, which in contrast have reduced activities (Cancer Chemothr. Pharmacol., 30, 51–57 (1992)). Also for the cardiac toxicity, amrubicin is far weaker than doxorubicin in rabbit chronic experimental model (Invest. New Drug, 15, 219–225 (1997)).
It has been known that, although anthracycline compounds have similar structures, they are different in their indications, action mechanisms and so on as described below. Daunorubicin and idarubicin are approved for treatment of leukemia but are not approved for treatment of solid cancers. On the other hand, doxorubicin, epirubicin, pirarubicin and aclarubicin are approved for treatment of solid cancers. Daunorubicin and doxorubicin inhibit synthesis of DNA and synthesis of RNA in similar degrees but aclarubicin and marcellomycin inhibit synthesis of RNA more strongly than synthesis of DNA; therefore their mechanism of exerting antitumor activities are quite different (JJSHP, 27, 1087–1110 (1991)). It has been known that, in this manner, even if drugs belong to the same category of anthracycline, they have different effect depending on the kind of cancer, and the same anticancer agent has different effect depending on the kind of cancer. Consequently, it is necessary to specifically confirm by experiment whether or not a specific anticancer agent is effective against a specific tumor (cancer).
It has been described that a use of amrubicin hydrochloride in combination with cisplatin or the like exhibits an additive effect on human T-cell leukemia MOLT-3 cell strain and human osteosarcoma MG-63 cell strain (Investigational New Drugs, 14, 357–363 (1996)). Additionally, an effect has been described, in an experiment with murine leukemia P388 cell strain, for a combined use of amrubicin and cisplatin in vivo (Yoshikazu YANAGI et al., Abstracts of publications in Japanese Cancer Association, No. 2168 (1989)). No report, however, has been described for a combined use of amrubicin and another medicament for treating lung cancer against lung cancer and for side effects.